scholarly journals The levels of neurofilament light at admission and development of axonal pathology in mild traumatic brain injury

2021 ◽  
Vol 1 ◽  
pp. 100615
Author(s):  
I. Hossain ◽  
M. Mohammadian ◽  
H.-R. Maanpää ◽  
R. Takala ◽  
O. Tenovuo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Neurofilament Light ◽  
Axonal Pathology

scholarly journals Diverse changes in microglia morphology and axonal pathology during the course of 1 year after mild traumatic brain injury in pigs

2021 ◽  
Author(s):  
Michael R. Grovola ◽  
Nicholas Paleologos ◽  
Daniel P. Brown ◽  
Nathan Tran ◽  
Kathryn L. Wofford ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Axonal Pathology ◽  
Microglia Morphology

Temporal profile and utility of serum neurofilament light in a rat model of mild traumatic brain injury

2021 ◽  
Vol 341 ◽  
pp. 113698
Author(s):  
William T. O'Brien ◽  
Louise Pham ◽  
Rhys D. Brady ◽  
Jesse Bain ◽  
Glenn R. Yamakawa ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Rat Model ◽  
Neurofilament Light ◽  
Temporal Profile

scholarly journals Early Levels of Glial Fibrillary Acidic Protein and Neurofilament Light Protein in Predicting the Outcome of Mild Traumatic Brain Injury

2019 ◽  
Vol 36 (10) ◽  
pp. 1551-1560 ◽  
Author(s):  
Iftakher Hossain ◽  
Mehrbod Mohammadian ◽  
Riikka S.K. Takala ◽  
Olli Tenovuo ◽  
Linnéa Lagerstedt ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glial Fibrillary Acidic Protein ◽  
Mild Traumatic Brain Injury ◽  
Acidic Protein ◽  
Neurofilament Light

scholarly journals Diverse Changes in Microglia Morphology and Axonal Pathology Over One Year after Mild Traumatic Brain Injury in Pigs

2020 ◽  
Author(s):  
Michael R. Grovola ◽  
Nicholas Paleologos ◽  
Daniel P. Brown ◽  
Nathan Tran ◽  
Kathryn L. Wofford ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Mild Traumatic Brain Injury ◽  
Periventricular White Matter ◽  
Post Injury ◽  
Mild Tbi ◽  
Time Points ◽  
Axonal Pathology ◽  
The Brain

AbstractOver 2.8 million people experience mild traumatic brain injury (TBI) in the United States each year, which may lead to long-term neurological dysfunction. The mechanical forces that occur due to TBI propagate through the brain to produce diffuse axonal injury (DAI) and trigger secondary neuroinflammatory cascades. The cascades may persist from acute to chronic time points after injury, altering the homeostasis of the brain. However, the relationship between the hallmark axonal pathology of diffuse TBI and potential changes in glial cell activation or morphology have not been established in a clinically relevant large animal model at chronic time points. In this study, we assessed tissue from pigs subjected to rapid head rotation in the coronal plane to generate mild TBI. Neuropathological assessments for axonal pathology, microglial morphological changes, and astrocyte reactivity were conducted in specimens out to 1 year post injury. We detected an increase in overall amyloid precursor protein pathology, as well as periventricular white matter and fimbria/fornix pathology after a single mild TBI. We did not detect changes in corpus callosum integrity or astrocyte reactivity. However, detailed microglial skeletal analysis revealed changes in morphology, most notably increases in the number of microglial branches, junctions, and endpoints. These subtle changes were most evident in periventricular white matter and certain hippocampal subfields, and were observed out to 1 year post injury in some cases. These ongoing morphological alterations suggest persistent change in neuroimmune homeostasis. Additional studies are needed to characterize the underlying molecular and neurophysiological alterations, as well as potential contributions to neurological deficits.

scholarly journals White Matter Tract Integrity: An Indicator of Axonal Pathology after Mild Traumatic Brain Injury

2018 ◽  
Vol 35 (8) ◽  
pp. 1015-1020 ◽  
Author(s):  
Sohae Chung ◽  
Els Fieremans ◽  
Xiuyuan Wang ◽  
Nuri E. Kucukboyaci ◽  
Charles J. Morton ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Mild Traumatic Brain Injury ◽  
White Matter Tract ◽  
Axonal Pathology

scholarly journals Blood biomarkers for mild traumatic brain injury: a selective review of unresolved issues

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Daniel B. Hier ◽  
Tayo Obafemi-Ajayi ◽  
Matthew S. Thimgan ◽  
Gayla R. Olbricht ◽  
Sima Azizi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Ct Scan ◽  
Mild Traumatic Brain Injury ◽  
Current Knowledge ◽  
Blood Biomarkers ◽  
Predictive Capacity ◽  
Neurofilament Light Chain ◽  
Neurofilament Light ◽  
Blood Biomarker

Abstract Background The use of blood biomarkers after mild traumatic brain injury (mTBI) has been widely studied. We have identified eight unresolved issues related to the use of five commonly investigated blood biomarkers: neurofilament light chain, ubiquitin carboxy-terminal hydrolase-L1, tau, S100B, and glial acidic fibrillary protein. We conducted a focused literature review of unresolved issues in three areas: mode of entry into and exit from the blood, kinetics of blood biomarkers in the blood, and predictive capacity of the blood biomarkers after mTBI. Findings Although a disruption of the blood brain barrier has been demonstrated in mild and severe traumatic brain injury, biomarkers can enter the blood through pathways that do not require a breach in this barrier. A definitive accounting for the pathways that biomarkers follow from the brain to the blood after mTBI has not been performed. Although preliminary investigations of blood biomarkers kinetics after TBI are available, our current knowledge is incomplete and definitive studies are needed. Optimal sampling times for biomarkers after mTBI have not been established. Kinetic models of blood biomarkers can be informative, but more precise estimates of kinetic parameters are needed. Confounding factors for blood biomarker levels have been identified, but corrections for these factors are not routinely made. Little evidence has emerged to date to suggest that blood biomarker levels correlate with clinical measures of mTBI severity. The significance of elevated biomarker levels thirty or more days following mTBI is uncertain. Blood biomarkers have shown a modest but not definitive ability to distinguish concussed from non-concussed subjects, to detect sub-concussive hits to the head, and to predict recovery from mTBI. Blood biomarkers have performed best at distinguishing CT scan positive from CT scan negative subjects after mTBI.

scholarly journals Plasma glial fibrillary acidic protein and neurofilament light chain, but not tau, are biomarkers of sports-related mild traumatic brain injury

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Etienne Laverse ◽  
Tong Guo ◽  
Karl Zimmerman ◽  
Martha S Foiani ◽  
Bharat Velani ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Glial Fibrillary Acidic Protein ◽  
Mild Traumatic Brain Injury ◽  
Light Chain ◽  
Acidic Protein ◽  
Post Injury ◽  
Neurofilament Light Chain ◽  
Neurofilament Light

Abstract Mild traumatic brain injury is a relatively common event in contact sports and there is increasing interest in the long-term neurocognitive effects. The diagnosis largely relies on symptom reporting and there is a need for objective tools to aid diagnosis and prognosis. There are recent reports that blood biomarkers could potentially help triage patients with suspected injury and normal CT findings. We have measured plasma concentrations of glial and neuronal proteins and explored their potential in the assessment of mild traumatic brain injury in contact sport. We recruited a prospective cohort of active male rugby players, who had pre-season baseline plasma sampling. From this prospective cohort, we recruited 25 players diagnosed with mild traumatic brain injury. We sampled post-match rugby players without head injuries as post-match controls. We measured plasma neurofilament light chain, tau and glial fibrillary acidic protein levels using ultrasensitive single molecule array technology. The data were analysed at the group and individual player level. Plasma glial fibrillary acidic protein concentration was significantly increased 1-h post-injury in mild traumatic brain injury cases compared to the non-injured group (P = 0.017). Pairwise comparison also showed that glial fibrillary acidic protein levels were higher in players after a head injury in comparison to their pre-season levels at both 1-h and 3- to 10-day post-injury time points (P = 0.039 and 0.040, respectively). There was also an increase in neurofilament light chain concentration in brain injury cases compared to the pre-season levels within the same individual at both time points (P = 0.023 and 0.002, respectively). Tau was elevated in both the non-injured control group and the 1-h post-injury group compared to pre-season levels (P = 0.007 and 0.015, respectively). Furthermore, receiver operating characteristic analysis showed that glial fibrillary acidic protein and neurofilament light chain can separate head injury cases from control players. The highest diagnostic power was detected when biomarkers were combined in differentiating 1-h post-match control players from 1-h post-head injury players (area under curve 0.90, 95% confidence interval 0.79–1.00, P < 0.0002). The brain astrocytic marker glial fibrillary acidic protein is elevated in blood 1 h after mild traumatic brain injury and in combination with neurofilament light chain displayed the potential as a reliable biomarker for brain injury evaluation. Plasma total tau is elevated following competitive rugby with and without a head injury, perhaps related to peripheral nerve trauma and therefore total tau does not appear to be suitable as a blood biomarker.

scholarly journals Poor sleep correlates with biomarkers of neurodegeneration in mild traumatic brain injury patients: a CENC Study

SLEEP ◽  
2020 ◽  
Author(s):  
J Kent Werner ◽  
Pashtun Shahim ◽  
Josephine U Pucci ◽  
Lai Chen ◽  
Sorana Raiciulescu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Executive Function ◽  
Brain Injury ◽  
Cognitive Function ◽  
Sleep Quality ◽  
Mild Traumatic Brain Injury ◽  
Poor Sleep ◽  
Neurofilament Light ◽  
Therapeutic Implications ◽  
Obstructive Sleep

Abstract Study Objectives Sleep disorders affect over half of mild traumatic brain injury (mTBI) patients. Despite evidence linking sleep and neurodegeneration, longitudinal TBI-related dementia studies have not considered sleep. We hypothesized that poor sleepers with mTBI would have elevated markers of neurodegeneration and lower cognitive function compared to mTBI good sleepers and controls. Our objective was to compare biomarkers of neurodegeneration and cognitive function with sleep quality in warfighters with chronic mTBI. Methods In an observational warfighters cohort (n=138 mTBI, 44 controls), the Pittsburgh Sleep Quality Index (PSQI) was compared with plasma biomarkers of neurodegeneration and cognitive scores collected an average of 8 years after injury. Results In the mTBI cohort, poor sleepers (PSQI≥10, n = 86) had elevated plasma neurofilament light (NfL, x̅ = 11.86 vs. 7.91 pg/mL, p=0.0007, d=0.63) and lower executive function scores by the categorical fluency (x̅ = 18.0 vs 21.0, p=0.0005, d= -0.65) and stop-go tests (x̅ = 30.1 vs 31.1, p=0.024, d = -0.37). These findings were not observed in controls (n = 44). PSQI predicted NfL (Beta=0.22, p=0.00002) and tau (Beta=0.14, p=0.007), but not amyloid β42. Poor sleepers showed higher obstructive sleep apnea (OSA) risk by STOP-BANG scores (x̅ = 3.8 vs 2.7, p=0.0005), raising the possibility that the PSQI might be partly secondary to OSA. Conclusions Poor sleep is linked to neurodegeneration and select measures of executive function in mTBI patients. This supports implementation of validated sleep measures in longitudinal studies investigating pathobiological mechanisms of TBI related neurodegeneration, which could have therapeutic implications.

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